The present invention relates to methods and articles for treatment of periodontal disease, in particular to methods and articles for inhibiting periodontal pocket formation and healing periodontal defects. The present invention also provides method and articles for treatment of bony defects. Although examples described herein relate to bone defects in the mouth, similar treatment is applicable throughout the human body.
Periodontal disease is a disease of the periodontium, the tissues that invest and support the teeth as shown in FIG. 1. These tissues include: Gingiva 1, the soft gum tissue of the mouth; gingival epithelium 2, the protective surface layer of the gingiva which seals against the tooth where the tooth passes into the oral cavity; the cementum (not designated in FIG. 1), a natural adhesive covering the tooth root; alveolar bone 3, the bone of the jaw surrounding the tooth root; and the periodontal ligament 4, connective tissue which suspends and supports the tooth between alveolar bone and the tooth root.
The gingival tissue surrounding a healthy adult tooth, as illustrated in FIG. 2, forms a sulcus 5 where it attaches to the tooth. In the early stages of periodontal disease, the bacteria break down the attachment of the gingival epithelium to the tooth, forcing the epithelium to reattach apically (toward the root) away from infected tissue. Because the tissue is compromised by disease, the new attachment is weak. Further infection progressively moves the attachment apically until the tooth is surrounded by a loose sleeve of diseased gingiva creating a pocket which is much deeper than the normal sulcus. As depicted in FIG. 3, the loose sleeve, called a periodontal pocket 6, is difficult to clean because a tooth brush and floss cannot reach the bacteria and plaque which accumulate within the pocket. As disease extends the periodontal pocket, the cementum, periodontal ligament, and supporting alveolar bone are destroyed, leaving a periodontal defect 7 filled with plaque and bacteria. Eventual the loss of the supporting periodontium leads to loss of the tooth.
Periodontal disease is the most common disease known to man. It is reported in the literature that it affects 75 percent of the adult population and is the major reason for tooth loss after the age of 35, and that fifty-five million teeth are lost to the disease each year in the United States.
Conventional treatment of periodontal defects consists of attempts to surgically alter the periodontal pocket morphology or obtain coronal (toward the crown) reattachment of the gingiva to the tooth. One prior art method alters the periodontal pocket morphology, creating a normally-shaped pocket at a site apical to the original attachment. This is accomplished by cutting away the coronal gingival tissue of a periodontal pocket and, if necessary, reshaping the underlying bone, to create a periodontal pocket similar in depth to a normal sulcus so that regular oral hygiene might be used to maintain the attachment of the gingiva to the tooth. This treatment does not recreate the coronal attachment of gingiva to the tooth maintained before the diseased condition and does not replace periodontium lost to the disease.
In another conventional treatment known as a gingival flap procedure, one or more flaps of gingival tissue are dissected away from the tooth. After the tooth is thoroughly cleaned by scaling or curetting; the flaps are reapposed to the tooth, some times incorporating gingival grafts from other portions of the mouth. However, reattachment of gingiva to a tooth surface that has been diseased is difficult to obtain using this procedure. Gingival epithelium migrates rapidly along the tooth root surface toward the apex of the tooth. Because bone and the periodontal ligament heal much more slowly than the migrating epithelium, the epithelium often migrates apically back to the presurgical level recreating a periodontal pocket similar in dimension to the pocket before treatment. Although the flap procedure is commonly used by clinicians, it is mostly successful with three wall defects (referring to the number of bony walls left surrounding defect); less successful with two wall defects, and not at all successful with one wall defect (Ellegaard, B., Karring, T. and Loe, H. "New periodontal attachment procedure based on retardation of epithelial migration," J. Clinical Periodontology 74:1:75-88).
Historically, investigators have attempted to improve upon the treatment of periodontal disease by encouraging the attachment of gingival tissue to the tooth, speeding the healing of gingival tissue from a healing defect site. By etching the tooth root surface with acids, some researchers have attempted to cause the gingival connective tissue (the highly vascular connective structure of the gingiva) to attach to the tooth, thus stopping the apical migration of gingival epithelium. Other researchers have attempted to fill bony defects with autogenous bone or artificial bone substitutes such as hydroxylapatite or tricalcium phosphate so that the bony portion of the defect might heal despite the rapid apical spread of epithelium. In another treatment, foils or other membranes into which gingival tissue cannot penetrate are used to separate the gingival tissue from the healing defect. In this method, the epithelium migrates apically along one side of the membrane or foil, while the defect heals on the opposite side of the membrane.
Previous attempts to correct periodontal defects with synthetic materials have not provided for the attachment of gingival tissue to the tooth while controlling the apical migration of epithelium. For this reason, these techniques have met with only limited success. Ideally periodontal disease should be treated by obtaining an attachment of gingival tissue to the tooth which will halt the apical migration of epithelium near the level maintained before the disease. The defect apical to the gingival attachment can then be healed in by the appropriate periodontal tissues.
A bony defect is any unnatural or irregular anatomy of the bone structure, particularly where bone is missing from the natural anatomy. Bone defects are commonly found in the oral cavity including the jaw bone, and are often the result of traumatic injury to the teeth and bone, disease affecting pulp canals of the teeth, periodontal disease, tooth root fractures, tumors or cancer, or congenital defects.
These defects may be functional or aesthetic in nature and have been treated in the past by grafting either natural or synthetic materials to increase tissue volume. The natural grafting materials include iliac, rib, or oral bone harvested from the patient who will receive the graft (i.e. autogenous), cortical or cancellous bone harvested from an individual different from the patent (i.e., allogenous), or cortical or cancellous bone harvested from a different mammalian species (i.e. xenogenous). Synthetic materials include particles or blocks of either solid or porous hydroxylapatite, particles or blocks of synthetic polymers such as poly (methylmethacrylate) or processed collagenous material usually obtained from a bovine source.
There are two major difficulties associated with the use of the above materials. First, none of the above-mentioned materials predictably result in resolution of the bony defect with viable bone tissue. Autogenous iliac grafts result in the most predictable bone healing, but require a painful surgical procedure to harvest the iliac graft material.
After surgical placement of any of the above mentioned graft materials into a bone defect, bone cells and fibrous connective tissue cells compete to fill the void space within the graft material or to replace the graft material as it resorbs. Because fibrous connective tissue can grow and form faster than bone tissue, the above-mentioned graft materials may attach or be partly ingrown with bone; however, the majority of healing is accomplished by ingrowth of soft connective tissue. In addition, with particulate materials, the particles tend to migrate over time through the soft tissue beyond the margins of the bone defect thereby reducing or minimizing therapeutic results.
The second major problem is that all of the above-mentioned materials are prone to either dehiscence of the suture line due to stretching the gingival tissue over them during closure of the surgical site or perforation of the graft material through the gingival tissue at some point after initial healing has occurred In either case, exposure of the graft material occurs with subsequent infection and loss of graft material.